ArticleInternational journal of medical sciences2017
IL-36γ inhibits differentiation and induces inflammation of keratinocyte via Wnt signaling pathway in psoriasis.
Article in International journal of medical sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 92 citations in OpenAlex.
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- Molecular Insights into HPV-Driven Cervical Cancer: Oncoproteins, Immune Evasion, and Epigenetic Modifications.Microorganisms · 2025Review
- Vaginal Microbiota and Local Immunity in HPV-Induced High-Grade Cervical Dysplasia: A Narrative Review.International journal of molecular sciences · 2025Review
- IWR-1 attenuates the promotional effect of IL-36γ in a mouse model of psoriasis.BMC immunology · 2024Article
- Interleukin-36 Is Highly Expressed in Skin Biopsies from Two Patients with Netherton Syndrome.Dermatopathology (Basel, Switzerland) · 2024Article
- Generalized Pustular Psoriasis and Systemic Organ Dysfunctions.International journal of molecular sciences · 2024Review
- ΔNp63 Regulates Homeostasis, Stemness, and Suppression of Inflammation in the Adult Epidermis.The Journal of investigative dermatology · 2024Article
- Sublingual Immunotherapy Decreased the Serum Levels of Interleukin-36Mediators of inflammation · 2024Article
- Role of ErbB and IL-1 signaling pathways in the dermonecrotic lesion induced by Loxosceles sphingomyelinases D.Archives of toxicology · 2023Article
- Luteolin alleviated neutrophilic asthma by inhibiting IL-36γ secretion-mediated MAPK pathways.Pharmaceutical biology · 2023Article
- Thymic mimetic cells function beyond self-tolerance.Nature · 2023Article
- Challenges and Future Trends in Atopic Dermatitis.International journal of molecular sciences · 2023Review
- Targeting TGF-β1/miR-21 Pathway in Keratinocytes Reveals Protective Effects of Silymarin on Imiquimod-Induced Psoriasis Mouse Model.JID innovations : skin science from molecules to population health · 2023Article
- Inflammation modulates intercellular adhesion and mechanotransduction in human epidermis via ROCK2.iScience · 2023Article
- Research Progress of mBioMed research international · 2023Review
- Gene set enrichment analysis and ingenuity pathway analysis to verify the impact of Wnt signaling in psoriasis treated with Taodan granules.American journal of translational research · 2023Article
- Exploring the Molecular Pathogenesis, Pathogen Association, and Therapeutic Strategies against HPV Infection.Pathogens (Basel, Switzerland) · 2022Review
- Immunometabolic profiling of cervicovaginal lavages identifies key signatures associated with adenomyosis.iScience · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a common inflammatory skin disease characterized by abnormal keratinocyte inflammation and differentiation that has a major impact on patients' quality of life. IL-36γ, a member of IL-36 cytokine family, is highly expressed in psoriasis and plays an important role in inflammation response and differentiation. However, the function of IL-36γ in differentiation and inflammation of keratinocyte in psoriasis has not been clearly identified. Thus, this study aimed to investigate the role of IL-36γ on differentiation and inflammation in HaCaT cells. HaCaT cells were divided into three groups: (1) Control group; (2) IL-36γ (100 ng/mL) group; (3) IL-36γ (100 ng/mL) + IWP-2 (1μM) group. Real time PCR was used to detect gene expression; the inflammation cytokines were examined by ELISA. We showed that treatment of HaCaT cells with IL-36γ significantly upregulated the expression levels of β-catenin, cyclin D1, and ki-67. IL-36γ also promoted the production of the inflammatory cytokines IFN-γ, IL-1β and IL-6, suppressed the expression of filaggrin, involucrin, keratin 1 and keratin 5. Meanwhile, we demonstrated the role of IWP-2, an inhibitor of the Wnt signaling pathway, in IL-36γ-treated HaCaT cells. Collectively, our findings suggest that IL-36γ inhibits differentiation and induces inflammation of keratinocyte via Wnt signaling pathway in psoriasis, this indicated that downregulation of IL-36γ may be a potential therapeutic option in psoriasis.
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